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At least 19 recordsLinked to original sources

PubMed2004

Lysophospholipid generation and phosphatidylglycerol depletion in phospholipase A(2)-mediated surfactant dysfunction.

Pulmonary surfactant's complex mixture of phospholipids and proteins reduces the work of breathing by lowering alveolar surface tension during respiration. One mechanism of surfactant damage appears to be the hydrolysis of phospholipid by phospholipases activated in the inflamed lung. Humans have several candidate secretory phospholipase A(2) (sPLA(2)) enzymes in lung cells and infiltrating leukocytes that could damage extracellular surfactant. We considered two mechanisms of surfactant disruption by five human sPLA(2)s, including generation of lysophospholipids and the depletion of specific phospholipids. All five sPLA(2)s studied ultimately caused surfactant dysfunction. Each enzyme exhibited a different pattern of hydrolysis of surfactant phospholipids. Phosphatidylcholine, the major phospholipid in surfactant and the greatest potential source for generation of lysophospholipids, was susceptible to hydrolysis by group IB, group V, and group X sPLA(2)s, but not group IIA or IID. Group IIA hydrolyzed both phosphatidylethanolamine and phosphatidylglycerol, whereas group IID was active against only phosphatidylglycerol. Thus, with groups IB and X, the generation of lysophospholipids corresponded with surfactant dysfunction. However, hydrolysis of and depletion of phosphatidylglycerol had a greater correlation with surfactant dysfunction for groups IIA and IID. Surfactant dysfunction caused by group V sPLA(2) is less clear and may be the combined result of both mechanisms.

Animals↗

PubMed1997

Pulmonary clearance of 99mTc-DTPA in experimental surfactant dysfunction treated with surfactant instillation.

BACKGROUND: Breakdown of the alveolo-capillary barrier is a characteristic feature of respiratory distress syndrome. Restoration of alveolo-capillary barrier function may be an important aspect of surfactant replacement therapy. We examined the effect of surfactant instillation on alveolo-capillary barrier function in an experimental model of surfactant dysfunction by measuring pulmonary clearance of 99mTc-DTPA. METHODS: Nineteen rabbits were tracheotomized and mechanically ventilated. Surfactant dysfunction was induced by administration of a synthetic detergent in aerosol form. Detergent was given to 13 rabbits; seven rabbits were then treated with instillation of natural surfactant, whereas six rabbits received saline. Six rabbits were used as untreated controls. An aerosol of 99mTc-DTPA was administered to all animals and the pulmonary clearance was measured with a gamma camera. RESULTS: 99mTc-DTPA cleared from the lungs with a half-life of 71 +/- 22 min in the control animals, 21.4 +/- 7.4 min in the surfactant-treated animals and 5.8 +/- 1.5 min in the saline-treated animals. The difference in half-life between groups was highly significant (P < 0.001). There was no change in arterial oxygenation or compliance in controls or in animals treated with saline. In animals treated with surfactant, a small transient reduction in arterial oxygen tension and a more long-standing reduction in compliance were observed. CONCLUSION: Surfactant treatment thus significantly attenuated the effect of detergent treatment but did not restore alveolo-capillary transfer of 99mTc-DTPA to normal.

Animals↗

PubMed1997

Prediction of surfactant dysfunction in term infants by the click test.

Pulmonary surfactant dysfunction (inactivation, deficiency) has been implicated in term neonates with respiratory failure. This study has evaluated the click test, a biophysical test for surfactant function, which will be useful in rapidly and reliably identifying term neonates with surfactant dysfunction. Samples of tracheal and or gastric aspirates (0.2 ml) from 55 neonates, varying from 36 to 42 weeks of gestational age, with respiratory distress and fractional inspired oxygen concentration requirements of > 0.5 were shaken with 95% ethanol. Once bubbles formed the samples were examined in air-free water under a microscope. In a positive click test, the bubbles rhythmically increase and then decrease in size, denoting the presence of active surfactant. When few bubbles were observed, the specimen was labelled as equivocal, and if none were seen, it was called negative. Surfactant dysfunction (negative or equivocal test) was consistently seen in respiratory distress syndrome (RDS), transient tachypnea of the newborn, and severe meconium aspiration syndrome (MAS). Preliminary data suggest that the click test will provide a rapid and early diagnosis of surfactant dysfunction in term neonates. This should facilitate early treatment with exogenous surfactant in RDS, by early diagnosis of surfactant deficiency, and provide justification for immediate and ongoing surfactant treatment in newborns with MAS. The click test can provide a diagnostic tool for surfactant dysfunction and deficiency in randomized controlled trials of therapy in those disease states in which exogenous surfactant therapy may be useful.

Biophysical Phenomena↗

PubMedDate not supplied

Mechanisms of surfactant dysfunction in early acute lung injury.

Surfactant dysfunction that occurs during acute lung injury is associated with alterations in phospholipid, total protein, and surfactant apoprotein content. The functional importance of these changes was examined by characterizing the biophysical properties and biochemical composition of lung surfactant from endotoxin-treated guinea pigs (LPS) with acute lung injury. Static and dynamic lung compliance significantly decreased following endotoxin exposure. Lavage fluid demonstrated a neutrophil predominance, and tissue histopathology revealed inflammation consistent with acute lung injury. LPS surfactant isolated by ultracentrifugation had minimum surface tensions of 21 dynes/cm compared to 2 dynes/cm among control samples. Biochemical abnormalities in LPS surfactant included increased total protein, decreased phosphatidylcholine, and increased sphingomyelin, phosphatidylethanolamine, and lysophosphatidylcholine. The addition to normal guinea pig surfactant of butanol extracts precipitated from lavage fluid of LPS animals and containing known amounts of protein caused elevations in minimum surface tensions to > or = 20 dynes/cm at protein to phospholipid ratios equivalent to those observed in LPS surfactant pellets. Addition of equal amounts of precipitate isolated from control animals had no effect on interfacial properties. Furthermore, addition of lysophosphatidylcholine and sphingomyelin to normal surfactant to simulate composition changes observed in LPS surfactant had minimal effect on surface film behavior. The results support the hypothesis that aqueous soluble inhibitors of surfactant are generated within the alveolar compartment during acute inflammation, and that surfactant dysfunction cannot be accounted for on the basis of phospholipid composition changes.

Animals↗

PubMed2003

Progressive lung disease and surfactant dysfunction with a deletion in surfactant protein C gene.

Mutations in the surfactant protein (SP)-C gene are responsible for familial and sporadic interstitial lung disease (ILD). The consequences of such mutations on pulmonary surfactant composition and function are poorly understood. To determine the effects of a mutation in the SP-C gene on surfactant, we obtained lung tissue at the time of transplantation from a 14-mo-old infant with progressive ILD. An in-frame 9-bp deletion spanning codons 91-93 in Exon 3 of the SP-C gene was present on one allele; neither parent carried this deletion. SP-C mRNA was present in normal size and amount. By immunofluorescence, proSP-C was aggregated within alveolar Type II cells in a compartment separate from SP-B. In airway surfactant, there was little or no mature SP-B or SP-C; SP-A content was increased. Minimum surface tension was increased (20 mN/m, normal < 5 mN/m). Type II cells contained normal and disorganized appearing lamellar bodies by electron microscopy. This spontaneous deletion on one allele of the SP-C gene was associated with sporadic ILD and abnormalities in surfactant composition and function. We propose that a dominant negative effect on surfactant protein metabolism and function results from aggregation of misfolded proSP-C and subsequent cell injury and inflammation.

Adult↗

PubMed1993

Pulmonary clearance of tracers with different lipid and water solubility in experimental surfactant dysfunction.

We measured the pulmonary clearance of inhaled 99mTc-diethylenetriamine penta-acetic acid (DTPA), 99mTc-sestamibi and 99mTc-dimethyliminodiacetic acid (HIDA) in normal rabbits, and rabbits with surfactant dysfunction induced by the detergent dioctyl sodium sulfosuccinate. The tracers differ widely in lipid/water partition coefficients, but have similar molecular radius and weight. Five animals in each group received the detergent in aerosol, and the other five a vehicle aerosol, before the administration of the tracer. Pulmonary clearance of the tracers was measured with a gamma camera. The half-life of 99mTc-DTPA was 94 +/- 16 min in normal lungs, and 10 +/- 1 min after detergent administration (p < 0.001). The half-life for 99mTc-sestamibi was 45 +/- 4 min and 39 +/- 4 min, respectively, (p < 0.05). There was no significant difference between the half-life of 99mTc-HIDA in normal lungs and in lungs with surfactant dysfunction. The half-life was 20 +/- 3 min and 17 +/- 2 min, respectively. The results indicate that the clearance rate limiting factors for the alveolocapillary transfer of water and lipid soluble substances are not the same. Surfactant dysfunction affects the transfer of water soluble substances (99mTc-DTPA) but not of substances with high lipid solubility (99mTc-HIDA).

Aerosols↗

PubMed1996

Increased airway resistance due to surfactant dysfunction can be alleviated with aerosol surfactant.

To investigate the contribution of pulmonary surfactant to a low airflow resistance through narrow conducting airways, a system was developed with which it was possible to determine the resistance meeting a steady flow of air at 0.5 mL/min. The airflow, delivered by an infusion pump, entered the extreme periphery of a conducting airway in an excised rat lung and exited through the trachea. The resistance was determined by measuring the pressure of the air entering the lung. If the airway remained open, the pressure was only slightly above zero; when a blocking liquid column formed in the lumen of the airway, the pressure increased rapidly but dropped abruptly as the liquid was pushed away into a wider airway section. When endogenous pulmonary surfactant was removed with a saline lavage, the airway was blocked almost constantly by an endless re-formation of liquid columns. Consequently, during a 4-min period of pressure recording, free airflow was observed only rarely. However, administration of aerosol surfactant increased the duration of free airflow in relation to the volume administered. After an injection of 80 mL of aerosol surfactant, the airway stayed open 89 +/- 3% of the 4-min recording time compared with only 28 +/- 5% when the same volume of air (80 mL) without surfactant had passed through the airway (p < 0.0001). We conclude that surfactant contributes to a free airflow through conducting airways and may have an important role in the maintenance of low airway resistance.

Aerosols↗

PubMed1995

Surfactant dysfunction develops when the immunized guinea-pig is challenged with ovalbumin aerosol.

BACKGROUND: The cause of the airway resistance developing during an asthma attack is not completely understood. Besides bronchospasm and airway oedema a surfactant dysfunction has been suggested as a reason for an increased airway resistance. OBJECTIVE: This paper aims at examining if indeed surfactant dysfunction develops when an asthma attack is induced in guinea-pigs. METHODS: Guinea-pigs, immunized against ovalbumin and then challenged (by inhaling the antigen) underwent lung function tests (n = 7) and were compared with seven animals challenged, but not immunized. Lung lavage was carried out in three groups of guinea-pigs: controls, never immunized nor challenged (n = 7), not immunized but challenged (n = 6), immunized and challenged, no lung function test (n = 6). After concentrating the lavage fluid 10 times the surface activity was evaluated with the pulsating bubble surfactometer. The fluid's concentration of phospholipids and proteins was determined as was the phospholipid composition. RESULTS: The 19 immunized and challenged animals all developed severe respiratory distress, six so seriously that they died. Lung function tests showed significantly increased airway resistance and decreased tidal volume, minute volume, and dynamic compliance. Surface activity of lavage fluid from immunized and challenged animals was significantly reduced when compared with fluid from control animals (P < 0.01). Immunization and challenge had no effect on the lavage fluid's phospholipid concentration or composition, but the proteins were at a higher concentration than in the fluid of the controls (P < 0.01). CONCLUSION: Proteins leaking into the airways inhibited the surfactant. This, in turn might have caused conducting airways to become blocked by liquid columns, which would increase airway resistance.

Administration, Inhalation↗

PubMed2006

Surfactant dysfunction in SP-A-/- and iNOS-/- mice with mycoplasma infection.

Surfactant dysfunction was studied in C57BL/6 (B6), B6.SP-A(-/-), and B6.iNOS(-/-) mice with pulmonary mycoplasma infection (10(7) colony-forming units). Cell-free bronchoalveolar lavage (BAL) from uninfected B6.SP-A(-/-) versus B6 mice had a reduced content of very large aggregates (VLA) and an increase in intermediate large aggregates (ILA), with no difference in total large aggregates (LA = VLA + ILA). However, LA from uninfected B6.SP-A(-/-) versus B6 mice contained less protein and were more sensitive to inhibition by serum albumin and lysophosphatidylcholine in pulsating bubble studies in vitro. Infection with Mycoplasma pulmonis caused significant lung injury and surfactant abnormalities in B6.SP-A(-/-), B6.iNOS(-/-), and B6 mice at 24, 48, 72 h after infection compared with uninfected mice of the same strain. Analyses of time-pooled data indicated that mycoplasma-infected B6.SP-A(-/-) and B6.iNOS(-/-) mice had significantly lower levels of LA and higher protein/phospholipid ratios in BAL compared with infected B6 mice. Infected B6.iNOS(-/-) versus B6 mice also had increased minimum surface tensions on the pulsating bubble and decreased levels of surfactant protein (SP)-B in BAL. These results indicate that pulmonary mycoplasma infection in vivo causes lung injury and surfactant abnormalities that are dependent in part on iNOS and SP-A. In addition, SP-A deficiency modifies surfactant aggregate content and lowers the inhibition resistance of LA surfactant in vitro compared with congenic normal mice.

Animals↗

PubMed1996

Surfactant dysfunction after inhalation of nitric oxide.

To study whether nitric oxide (NO) affects surfactant function, 36 young rats inhaled one of the following humidified environments for 24 h: 1) air; 2) 95% O2; 3) air and 100 parts/million (ppm) NO; and 4) 95% O2 and 100 ppm NO. The treatments did not change the recovery of phospholipid from bronchoalveolar lavage (BAL). Exposure to NO of animals that breathed either air or 95% O2 increased the minimum surface tension of surfactant from BAL at low (1.5 mumol/ml), but not at high (4 mumol/ml), phosphatidylcholine concentration. After inhaled NO, the nonsedimentable protein of BAL decreased the surface activity of surfactant (1 mumol phosphatidylcholine/ml) more than the protein from the controls. NO treatment of animals that breathed either air or 95% O2 affected neither the quantity nor the molecular weight distribution of nonsedimentable protein. Hyperoxia increased the amount of the nonsedimentable protein, whereas NO increased the iron saturation of transferrin. The surfactant fraction and the nonsedimentable protein from BAL were separately exposed to 80 ppm NO in vitro. NO exposure had no effect on the surface activity of surfactant fraction. NO exposure of nonsedimentable protein from the control animals (no NO) increased the inhibition of the surface activity and changed the adsorption spectrum of the protein, suggesting conversion of hemoglobin to methemoglobin. Nonsedimentable protein from NO-exposed animals contained methemoglobin. We propose that surfactant dysfunction caused by inhaled NO is in part due to alteration of protein(s) in epithelial lining fluid that in turn inactivates surfactant.

Administration, Inhalation↗

PubMed2001

Decreased surfactant protein-B expression and surfactant dysfunction in a murine model of acute lung injury.

This study examines the relationships between inflammation, surfactant protein (SP) expression, surfactant function, and lung physiology in a murine model of acute lung injury (ALI). 129/J mice received aerosolized endotoxin lipopolysaccharide [LPS] daily for up to 96 h to simulate the cytokine release and acute inflammation of ALI. Lung elastance (E(L)) and resistance, lavage fluid cell counts, cytokine levels, phospholipid and protein content, and surfactant function were measured. Lavage and lung tissue SP content were determined by Western blot and immunohistochemistry, and tissue messenger RNA (mRNA) levels were assessed by Northern blot and in situ hybridization. Tumor necrosis factor-alpha and neutrophil counts in bronchoalveolar lavage fluid increased within 2 h of LPS exposure, followed by increases in total protein, interleukin (IL)-1beta, IL-6, and interferon-gamma. E(L) increased within 24 h of LPS exposure and remained abnormal up to 96 h. SP-B protein and mRNA levels were decreased at 24, 48, and 96 h. By contrast, SP-A protein and mRNA levels and SP-C mRNA levels were not reduced. Surfactant dysfunction occurred coincident with changes in SP-B levels. This study demonstrates that lung dysfunction in mice with LPS-ALI corresponds closely with abnormal surfactant function and reduced SP-B expression.

Animals↗

PubMed1997

Surfactant dysfunction develops in BALB/c mice infected with respiratory syncytial virus.

Recent reports suggest an important role for pulmonary surfactant in maintaining the patency of narrow conducting airways. The hypothesis that surfactant dysfunction is an important factor in respiratory syncytial virus (RSV) infection was tested in a mouse model. Mice, inoculated with either a low or a high dose of RSV, were subjected to bronchoalveolar lavage (BAL), and the fluids were analyzed for percentage of inflammatory cells and concentrations of proteins and phospholipids. After concentration of the surfactant by centrifugation, its function was analyzed with a capillary surfactometer. RSV infection resulted in a dose-dependent disruption of surfactant function (p < 0.0001). BAL fluid supernatants were added to calf lung surfactant extract (CLSE) to examine whether surfactant inhibiting agents were present. Indeed, BAL fluid supernatants of RSV-infected mice disrupted the normal function of calf lung surfactant extract in a dose dependent way (p < 0.0001), indicating the presence of inhibitors. Protein concentrations were increased in BAL fluids of RSV-infected mice versus control mice (p < 0.0001), and were inversely related to surfactant function (r = -0.44, p = 0.0004), suggesting an inhibitory effect of proteins. Protein concentration also correlated with the percentage of inflammatory cells (r = 0.51, p = 0.004). Phospholipid concentrations were not affected by the RSV infection. The results of these studies strongly suggest that a disruption of pulmonary surfactant function, most likely due to inhibition from inflammatory proteins, is important for the pathophysiology of RSV infection.

Animals↗

PubMed2005

Lung surfactant dysfunction in tuberculosis: effect of mycobacterial tubercular lipids on dipalmitoylphosphatidylcholine surface activity.

In pulmonary tuberculosis, Mycobacterium tuberculosis bacteria reside in the alveoli and are in close proximity with the alveolar surfactant. Mycolic acid in its free form and as cord factor, constitute the major lipids of the mycobacterial cell wall. They can detach from the bacteria easily and are known to be moderately surface active. We hypothesize that these surface-active mycobacterial cell wall lipids could interact with the pulmonary surfactant and result in lung surfactant dysfunction. In this study, the major phospholipid of the lung surfactant, dipalmitoylphosphatidylcholine (DPPC) and binary mixtures of DPPC:phosphatidylglycerol (PG) in 9:1 and 7:3 ratios were modelled as lung surfactant monolayers and the inhibitory potential of mycolic acid and cord factor on the surface activity of DPPC and DPPC:PG mixtures was evaluated using Langmuir monolayers. The mycobacterial lipids caused common profile changes in all the isotherms: increase in minimum surface tension, compressibility and percentage area change required for change in surface tension from 30 to 10 mN/m. Higher minimum surface tension values were achieved in the presence of mycolic acid (18.2+/-0.7 mN/m) and cord factor (13.28+/-1.2 mN/m) as compared to 0 mN/m, achieved by pure DPPC film. Similarly higher values of compressibility (0.375+/-0.005 m/mN for mycolic acid:DPPC and 0.197+/-0.003 m/mN for cord factor:DPPC monolayers) were obtained in presence of mycolic acid and cord factor. Thus, mycolic acid and cord factor were said to be inhibitory towards lung surfactant phospholipids. Higher surface tension and compressibility values in presence of tubercular lipids are suggestive of an unstable and fluid surfactant film, which will fail to achieve low surface tensions and can contribute to alveolar collapse in patients suffering from pulmonary tuberculosis. In conclusion a biophysical inhibition of lung surfactant may play a role in the pathogenesis of tuberculosis and may serve as a target for the development of new drug loaded surfactants for this condition.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1992

Pulmonary clearance of 99mTc--DTPA and 99mTc-albumin in rabbits with surfactant dysfunction and lung injury.

We measured the pulmonary clearance of inhaled 99mTc-DTPA and 99mTc-albumin in rabbits with surfactant dysfunction induced by dioctyl sodium sulphosuccinate and in rabbits with lung injury induced by oleic acid. The animals were tracheotomized and mechanically ventilated. After inhalation of 99mTc-albumin in ten animals, clearance of the tracer from the lungs was monitored for 90 min. The first 30 min was a control period. Dioctyl sodium sulphosuccinate was then administered in aerosol and after another 30 min oleic acid was injected intravenously. Ten other rabbits were given 99mTc-DTPA, and clearance was externally recorded for 60 min. Five animals inhaled detergent aerosol and five animals were given oleic acid intravenously after 30 min. Airway pressures, tidal volume, and arterial blood gases were measured before and after each intervention. The half-life of 99mTc-albumin in the lung was 442 +/- 123 min during the control period, 363 +/- 52 min after detergent administration, and 134 +/- 18 min after oleic acid administration (P less than 0.05 compared to control and P less than 0.01 compared to the period after detergent). The half-life of 99mTc-DTPA was 94 +/- 16 min before and 10 +/- 0.6 min (P less than 0.01) after detergent administration and 75 +/- 12 min before and 18 +/- 1.8 min (P less than 0.01) after oleic acid administration. Gas exchange was not affected by administration of dioctyl sodium sulphosuccinate but markedly impaired after injection of oleic acid. Compliance of the respiratory system remained unaffected by detergent but decreased after injection of oleic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

A mechanism of nitric oxide-induced surfactant dysfunction.

Inhaled nitric oxide (NO) may modify surfactant either by interacting with the surfactant complex or by changing the capacity of the proteins of the epithelial lining fluid to inhibit the surface activity. Natural surfactant was exposed to NO (80 parts/million) in air in vitro while the gas-liquid surface was cycled. In the presence or absence of oxidants (Fe2+, xanthine, xanthine oxidase), surfactant exposed to NO retained the high surface activity significantly better than control surfactants exposed to air. Two surfactant inhibitors, hemoglobin (Hb) and albumin, were separately exposed to NO. In contrast to albumin, NO-exposed Hb and methemoglobin (MetHb; 16-125 micrograms/ml) decreased the surface activity at low surfactant concentrations, whereas native Hb had no effect. Surfactant recovered by sedimentation after exposure to MetHb had decreased surface activity and contained MetHb, whereas Hb did not bind to surfactant. Acidic phospholipid phosphatidylglycerol increased the binding of MetHb to surfactant. The MetHb-induced decrease in surface activity was elicited in the presence of surfactant proteins, including a peptide mimicking surfactant protein B. MetHb (but not Hb) added to a low dose of exogenous surfactant decreased the efficacy of surfactant to improve the lung compliance of premature rabbits. We propose that inhaled NO promotes the surface activity of surfactant during tidal ventilation and that, in high-permeability lung edema and surfactant deficiency, inhaled NO increases the inhibition of surface activity by converting Hb to MetHb in the alveolar space.

Animals↗

PubMed1995

Surfactant dysfunction in lung preservation.

We studied the effect of lung preservation on the surfactant system in rats. Lung surfactant is necessary to maintain normal lung mechanics, and hence normal lung function. We evaluated lung mechanics with pressure-volume (P-V) curves, and analyzed biochemical changes of surfactant in bronchoalveolar lavage (BAL) fluid. Additionally, we determined wet to dry weight ratios (W/D). We defined five study groups. In group I (controls) we harvested lungs without pulmonary artery flushing, then evaluated them immediately. In group II we flushed lungs through the pulmonary artery (PA) with hypothermic modified Euro-Collins solution (mECS), then removed and studied them immediately to determine the consequences of PA flushing alone. In groups III, IV, and V we flushed lungs with mECS, then stored them in normal saline (NS) for 6 hr (group III); in NS for 12 hr (group IV); or in mECS for 12 hr (group V). In groups III, IV, and V we evaluated lungs after storage. All four experimental groups showed significant changes in lung mechanics and surfactant biochemistry, compared with controls. Lungs in groups III, IV, and V showed additional changes in lung mechanics and surfactant biochemistry compared with group II. The W/D in stored lungs (groups III, IV, and V) was significantly higher than in controls and group II. We conclude that lung preservation induces deleterious changes in the surfactant system. Surfactant alterations are evident immediately after pulmonary artery flushing, and increase in severity with storage.

Animals↗

PubMed1989

Protein leaks and surfactant dysfunction in the pathogenesis of respiratory distress syndrome.

This article reviews the phenomenon of surfactant inactivation by soluble proteins. Following surfactant treatment of preterm lambs, the initial clinical response was not maintained. The surface tensions that were low in the lungs following surfactant treatment increased to high values concurrently with the return of severe respiratory failure. The surface properties of the surfactant that remained in the airways and alveoli could be restored if the soluble proteins were removed. These soluble proteins inactivated different surfactants to different degrees and the interaction was very concentration dependent. The proteins entered the lungs of the preterm lamb because of the tendency of these lungs to form pulmonary oedema. Similar surfactant inactivation occurred in the lungs of infants with respiratory distress syndrome. A variety of manipulations influenced the formation of proteinaceous pulmonary oedema, suggesting that new therapeutic strategies could be developed to treat infants with RDS.

Humans↗

PubMed1996

Pulmonary surfactant dysfunction in congenital diaphragmatic hernia: experimental and clinical findings.

Experimental and clinical findings indicate immaturity of pulmonary surfactant in congenital diaphragmatic hernia (CDH). Lung histology has shown a decreased amount of lamellar bodies. A low lecithin/sphingomyelin ratio in the amniotic fluid, and decreased concentrations of surfactant protein A and disaturated phosphatidylcholine in the pulmonary tissue and the amniotic fluid have been reported. Furthermore, low compliance and high surface tension have also been found. Evidence of clinical and experimental findings of structural, biochemical and functional pulmonary immaturity in CDH is reviewed. Prenatal administration of corticosteroids to accelerate fetal pulmonary maturation, and the use of early surfactant therapy, should be further evaluated in the clinical management of CDH.

Adrenal Cortex Hormones↗